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BackgroundSpontaneous epidural hematoma (EDH) has been suggested associated with adjacent infective pathologies, dural vascular malformations, extradural metastasis, or coagulopathies. Cryptogenic spontaneous EDH is extremely rare. Case presentationWe reported a cryptogenic spontaneous EDH case in a young woman following sexual intercourse. She occurred consecutively EDH at three different sites within a short time. After three timely operations, a satisfactory outcome was achieved.Conclusion EDH should be investigated when a young patient develops headaches and signs of increased ICP after emotional hyperactivity or hyperventilation. If early diagnosis and surgical decompression can be carried out in time, the prognosis is satisfactory.

Objective Designing surgical strategies for ossified lesions in the upper cervical spine is challenging owing to the complex anatomic structures. The present study aimed to clarify the prevalence of ossified lesions in the upper cervical spine in patients with ossification in the posterior longitudinal ligament and illustrate the clinical features, radiological findings, and surgical outcomes of this abnormality. Methods Demographic and clinical data were collected for all patients preoperatively and included age, gender, body mass index, alcohol and tobacco use, history of diabetes, visual analog score, and Japanese Orthopaedic Association score. The cervical angle, morphology of ossification in the posterior longitudinal ligament, K-line, occupation ratio, space available for the spinal cord, high-intensity zone, and compression ratio of the spinal cord were calculated. The operative approach, technique used, and complications were recorded. Results A total of 38 patients were enrolled. The upper cervical segment in 23 patients was not surgically addressed. In the group with the upper cervical segment addressed surgically, 10 patients were treated with C3–C6 open-door laminoplasty and C2 partial laminectomy, 1 with C1–C7 laminoplasty, 1 with C2–C7 laminoplasty, 2 with C3–C6 total and C2 partial laminectomy, and 1 with C1–C5 laminectomy and occipitocervical fusion. Conclusions The development of ossified lesions in the upper cervical spine has a high incidence. Decompressive surgery for upper cervical spine segments should be recommended for patients with severe narrowing of the spinal canal and a high signal intensity that extends to the upper cervical segment of the spinal cord. We hope that the findings from the present study will aid in clinical decision-making and provide useful information that can be incorporated into future guidelines.

Study design Bibliometric and visualization analysis. Objective Lumbar spinal stenosis (LSS) has become a common health problem and the most frequent indication for spinal surgery. This study aimed to illustrate the overall knowledge structure, and development trends of LSS, using a bibliometric analysis and newly developed visualization tools. Materials and methods Research data sets were acquired from the Web of Science. The time span was defined as "2000-2019". VOS viewer and Citespace software was provided to analyze the data and generate visualization knowledge maps. Annual trend of publications, distribution, H-index status, co-authorship status and research hotspots were analyzed. Results A total of 1934 publications met the requirement. The United States published most papers (521, 26.9%), both total citations (17,626) and H-index (61) ranked first of all the countries. The most productive organizations on LSS is Seoul National University (50). Spine (43) published the most papers on LSS. Quality of life, risk factor, disability, double blind trials, and decompression surgery are the research hotspots in the recent years. Conclusion The number of publications showed an upward trend with a stable rise in recent years. The United States is a country with the highest productivity, not only in quality, but also in quantity. Seoul National University has been the largest contributor in this field. Spine is the best journal related to LSS. Quality of life, risk factor, disability, and decompression surgery are the research hotspots in the recent years. Indeed, this study provides a new insight to the growth and development of LSS. Moreover, it will contribute to the growth of the international frontier of LSS.

The clinical evidence indicated that cyclophosphamide (CPD), one of the chemotherapy drugs, caused severe deteriorations in bones of cancer patients. However, the exact mechanisms by which CPD exerts effects on bone remodeling is not yet fully elucidated. Therefore, this study was performed to investigate the role and potential mechanism of CPD in osteoblastogenesis and osteoclastogenesis. Here it was found that CPD treatment (100mg/kg/day) for 7 days led to osteoporosis phenotype in male mice. CPD inhibited osteoblastogenesis as shown by decreasing the number and differentiation of bone mesenchymal stem cells (MSCs) and reducing the formation and activity of osteoblasts. Moreover, CPD suppressed the osteoclastogenesis mediated by receptor activator for nuclear factor-κ B ligand (RANKL) as shown by reducing the maturation and activity of osteoclasts. At the molecular level, CPD exerted inhibitory effect on the expression of components (Cyclin D1, β-catenin, Wnt 1, Wnt10b) of Wnt/β-catenin signaling pathway in MSCs and osteoblasts-specific factors (alkaline phosphatase, Runx2, and osteocalcin). CPD also down-regulated the expression of the components (tumor necrosis factor receptor-associated factor 6, nuclear factor of activated T-cells cytoplasm 1, c-Fos and NF-κB) of RANKL signaling pathway and the factors (matrix metalloproteinase 9, cathepsin K, tartrate-resistant acid phosphates and carbonic anhydrase II) for osteoclastic activity. Taken together, this study demonstrated that the short-term treatment of CPD induced osteoporosis in mice and the underlying mechanism might be attributed to its marked suppression on osteoblastogenesis and osteoclastogenesis, especially the effect of CPD on bone formation might play a dominant role in its detrimental effects on bone remodeling.

The DOT1L histone H3 lysine 79 (H3K79) methyltransferase plays an oncogenic role in MLL-rearranged leukemogenesis. Here, we demonstrate that, in contrast to MLL-rearranged leukemia, DOT1L plays a protective role in ultraviolet radiation (UVR)-induced melanoma development. Specifically, the DOT1L gene is located in a frequently deleted region and undergoes somatic mutation in human melanoma. Specific mutations functionally compromise DOT1L methyltransferase enzyme activity leading to reduced H3K79 methylation. Importantly, in the absence of DOT1L, UVR-induced DNA damage is inefficiently repaired, so that DOT1L loss promotes melanoma development in mice after exposure to UVR. Mechanistically, DOT1L facilitates DNA damage repair, with DOT1L-methylated H3K79 involvement in binding and recruiting XPC to the DNA damage site for nucleotide excision repair (NER). This study indicates that DOT1L plays a protective role in UVR-induced melanomagenesis., The interaction of DOT1L with MLL oncogenic fusion proteins has been implicated in leukemogenesis. Here, the authors show a contrasting role for DOT1L in protecting UVR-induced melanomagenesis by facilitating DNA repair through interaction with XPC.

The anaphase-promoting complex or cyclosome with the subunit Cdh1 (APC/C(Cdh1)) is an E3 ubiquitin ligase involved in the control of the cell cycle. Here, we identified sporadic mutations occurring in the genes encoding APC components, including Cdh1, in human melanoma samples and found that loss of APC/C(Cdh1) may promote melanoma development and progression, but not by affecting cell cycle regulatory targets of APC/C. Most of the mutations we found in CDH1 were those associated with ultraviolet light (UV)-induced melanomagenesis. Compared with normal human skin tissue and human or mouse melanocytes, the abundance of Cdh1 was decreased and that of the transcription factor PAX3 was increased in human melanoma tissue and human or mouse melanoma cell lines, respectively; Cdh1 abundance was further decreased with advanced stages of human melanoma. PAX3 was a substrate of APC/C(Cdh1) in melanocytes, and APC/C(Cdh1)-mediated ubiquitylation marked PAX3 for proteolytic degradation in a manner dependent on the D-box motif in PAX3. Either mutating the D-box in PAX3 or knocking down Cdh1 prevented the ubiquitylation and degradation of PAX3 and increased proliferation and melanin production in melanocytes. Knocking down Cdh1 in melanoma cells in culture or before implantation in mice promoted doxorubicin resistance, whereas reexpressing wild-type Cdh1, but not E3 ligase-deficient Cdh1 or a mutant that could not interact with PAX3, restored doxorubicin sensitivity in melanoma cells both in culture and in xenografts. Thus, our findings suggest a tumor suppressor role for APC/C(Cdh1) in melanocytes and that targeting PAX3 may be a strategy for treating melanoma.

To further investigate the role of p53 in apoptosis in vivo and the interaction between p53 and Bcl-2 in the regulation of cellular apoptosis in vivo, we depleted p53 in Bcl-2-null mice. We found that the interaction between p53 and Bcl-2 are tissue dependent. Specifically, loss of p53 in Bcl-2-/- mice inhibits apoptotic induction in spleen and subsequently inhibits the Bcl-2-null-induced spleen atrophy. Furthermore, p53 deficiency overcomes loss of melanocyte stem cell (MSC)-induced apoptosis and subsequently prevents hair graying in Bcl-2- null mice. In addition, p53 deletion partly inhibits apoptosis in hair follicle keratinocytes, leading to the alleviation of hair growth delay in Bcl-2-null mice. However, p53 absence in Bcl-2-null mice cannot restore other defects in Bcl-2-null mice, including retardation of growth, short ears and polycystic kidney disease.

High levels of serum uric acid (SUAC) are frequently detected in patients with psoriasis. However, the relationship between psoriasis and hyperuricemia remains unknown. Here we conducted a meta-analysis to identify the SUAC levels in subjects with psoriasis and to determine whether there is an associated risk between psoriasis and hyperuricemia.A comprehensive search of the literature from January 1980 to November 2014 across 7 databases (MEDLINE, Embase, Cochrane Central Register, and 4 Chinese databases) was conducted to determine whether there is an associated risk between psoriasis and hyperuricemia.Among the 170 identified reports, 14 observational studies were included in this meta-analysis. We found a significant higher SUAC level (MD 0.68, 95% CI 0.26-1.09; P = 0.002) in patients with psoriasis in Western Europe, but no significant differences were found between the East Asia and India subgroup (MD 1.22, 95% CI -0.13-2.56; P = 0.08) or the Middle East subgroup (MD 0.48, 95% CI -0.49-1.44; P = 0.33). Similar results were obtained from the meta-analysis of SUAC levels in subjects with severe psoriasis.Our meta-analysis showed that the correlation between psoriasis and hyperuricemia was either ethnicity- or region-dependent and that patients with psoriasis in Western Europe were more likely to have hyperuricemia.